Pediatric Nephritis Treatment & Management
- Author: Sahar Fathallah-Shaykh, MD; Chief Editor: Craig B Langman, MD more...
Medical care for glomerulonephritis (GN) is usually divided into 2 major components: treatment of primary pathology and supportive care. In renal diseases, supportive care involves managing hypertension and fluid and electrolyte abnormalities and managing decreased renal function.
The treatment of primary pathology ranges from watchful waiting, as in postinfectious GN, to treatment with immunosuppressive medication, such as steroids or cyclophosphamide in lupus. To discuss the primary treatment of all forms of nephritis is beyond the scope of this article. In the case of some etiologies for GN, for example, IgM nephropathy, no definitive therapy is known.
Hypertension can be managed with antihypertensives, such as calcium channel–blocking agents, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor–blocking agents, peripheral vasodilators, and diuretics. The most common fluid abnormality, hypervolemia, is managed with fluid restriction and diuretics or with dialysis if renal function is too poor to respond to diuretics. Hyponatremia is usually dilutional and responds, at least partially, to removal of excess fluid. Hypocalcemia may respond to oral or IV calcium, depending on severity. Mild metabolic acidosis may be present but rarely requires primary treatment.
Some recommend a short course of steroids or cyclophosphamide for tubulointerstitial nephritis (TIN). Prednisone may speed up the recovery from renal symptoms of TIN. However, these drugs are usually not necessary. Most often, stopping the offending agent leads to recovery.
Primary care physicians can usually manage children with poststreptococcal GN unless dialysis is imminent. If dialysis access is necessary, consultation with a surgeon may be required. Refer children with other forms of GN or TIN to a pediatric nephrologist.
Inpatient care is usually necessary only to manage severe hypertension or complications of acute or chronic renal failure (eg, dialysis access, uremic syndrome, congestive heart failure, electrolyte abnormalities such as hyperkalemia and pericardial effusion). These problems are infrequent in the general pediatric population.
Children with renal failure should be cared for by a physician with experience in managing pediatric renal failure. In the United States, such doctors are frequently found at a tertiary facility.
Outpatient monitoring and care
Outpatient care may be as simple as observation in a child with tubulointerstitial nephritis (TIN) or resolving poststreptococcal glomerulonephritis (GN), or it may involve the use of antihypertensives, diuretics, and diet modification, as in a child with IgA nephropathy or membranoproliferative GN and preserved renal function. Outpatient therapy may involve dialysis in a child who develops end-stage renal disease.
Diet and Activity
In children with acute renal failure secondary to glomerulonephritis (GN) who have lost the ability to excrete a water load, fluid restriction may prevent fluid overload. Tubulointerstitial nephritis (TIN) usually produces nonoliguric acute renal failure. Fluid restriction of 300 mL/m2/d plus losses may allow management of acute renal failure for 2-3 days without dialysis. In patients with hypertension, sodium restriction to the recommended daily allowance (RDA) of 2-4 mEq/kg/d may aid in management. In children with renal failure, potassium restriction is justified to prevent hyperkalemia. A short-term high-carbohydrate diet may prevent catabolism of body protein as an energy source. Calcium supplementation is useful to maintain normal serum calcium.
In patients with hypertension and renal failure, discourage strenuous activity; however, walking, playing, and other activities are acceptable.
Wen YK, Chen ML. IgA-Dominant Postinfectious Glomerulonephritis: Not Peculiar to Staphylococcal Infection and Diabetic Patients. Ren Fail. 2011. 33(5):480-5. [Medline].
Vachvanichsanong P, McNeil E. Pediatric lupus nephritis: more options, more chances?. Lupus. 2013 Apr 29. [Medline].
Flanc RS, Roberts MA, Strippoli GF, et al. Treatment of diffuse proliferative lupus nephritis: a meta-analysis of randomized controlled trials. Am J Kidney Dis. 2004 Feb. 43(2):197-208. [Medline].
Endo A, Fuchigami T, Hasegawa M, Hashimoto K, Fujita Y, Inamo Y, et al. Posterior reversible encephalopathy syndrome in childhood: report of four cases and review of the literature. Pediatr Emerg Care. 2012 Feb. 28(2):153-7. [Medline].
Sfaihi L, Kamoun F, Hentati Y, Tiss O, Maaloul I, Kamoun T, et al. [Posterior reversible encephalopathy syndrome induced by acute postinfectious glomerulonephritis.]. Arch Pediatr. 2013 Apr 22. [Medline].
Goda C, Kotake S, Ichiishi A, et al. Clinical features in tubulointerstitial nephritis and uveitis (TINU) syndrome. Am J Ophthalmol. 2005. 140(4):637-41. [Medline].
Hettinga YM, Scheerlinck LM, Lilien MR, Rothova A, de Boer JH. The value of measuring urinary β2-microglobulin and serum creatinine for detecting tubulointerstitial nephritis and uveitis syndrome in young patients with uveitis. JAMA Ophthalmol. 2015 Feb. 133 (2):140-5. [Medline].
Jahnukainen T, Saarela V, Arikoski P, Ylinen E, Rönnholm K, Ala-Houhala M, et al. Prednisone in the treatment of tubulointerstitial nephritis in children. Pediatr Nephrol. 2013 Apr 19. [Medline].
Gonzalez B, Hernandez P, Olguin H, et al. Changes in the survival of patients with systemic lupus erythematosus in childhood: 30 years experience in Chile. Lupus. 2005. 14(11):918-23. [Medline].
Medjeral-Thomas NR, O'Shaughnessy MM, O'Regan JA, Traynor C, Flanagan M, Wong L, et al. C3 glomerulopathy: clinicopathologic features and predictors of outcome. Clin J Am Soc Nephrol. 2014 Jan. 9 (1):46-53. [Medline]. [Full Text].
Zhang Y, Nester CM, Martin B, Skjoedt MO, Meyer NC, Shao D, et al. Defining the complement biomarker profile of C3 glomerulopathy. Clin J Am Soc Nephrol. 2014 Nov 7. 9 (11):1876-82. [Medline].
Nicolas C, Vuiblet V, Baudouin V, Macher MA, Vrillon I, Biebuyck-Gouge N, et al. C3 nephritic factor associated with C3 glomerulopathy in children. Pediatr Nephrol. 2014 Jan. 29 (1):85-94. [Medline].